The mechanisms underlying the regulation of Akt and FOXO3a signaling during HCMV lytic and latent infection have not yet been fully elucidated, but our data demonstrate a role for miR-UL36, miR-UL112, and miR-UL148D in reducing Akt expression and signaling in hESC-derived CD34+ HPCs and thereby promoting FOXO3a activation and nuclear translocation. This evidence concerns the gene FOXO3 and disease arising from reactivation of latent virus.